Evidence of links between APLN/APJ and oxidative stress include the suppression by APLN/APJ of adipocyte-induced production and release of reactive oxygen species (ROS) and prevention of oxidative stress-linked cardiac hypertrophy; conversely, an active fragment of APLN can facilitate ROS generation in vascular smooth muscle cells, while APLN promotes the formation of atherosclerosis [9]. The gene discussed is APLNR; the disease is cardiac hypertrophy.